In preliminary studies we have shown that salt-hungry rats use information generated by sodium-specific elements in the liver to control their salt intake. The work proposed here will determine the contribution and context of this control relative to other mechanisms involved in the regulation of salt intake and sodium homeostasis. Our work and other research suggests the following tentative model: Ingested salt is slowly absorbed from the gastrointestinal tract and then carried by the hepatic-portal vein to the liver. the sodium is detected by sensors within the vein or liver, and the signal generated is relayed by afferent autonomic nerves to central integrative brainstem regions. These reduce subsequent salt intake, either directly, by modulating other brain regions, or indirectly, by ameliorating imbalances in the hormones of sodium homeostasis that cause salt hunger. We intend to test each stage of this model using salt-hungry rats to examine the following: (1) The relationship between salt intake and salt absorption, by measuring the appearance of sodium in the hepatic- portal vein after rats drink or administered various quantities of salt. (2) The effects on salt intake produced by pharmacological compromise of hepatic transduction. (3) The influence of disrupting transmission of information between the liver and brain by measuring salt intake of rats with selective liver denervations, and (4) the relationship between hepatic-portal levels of sodium and the hormones of sodium homeostasis.